The term “hepatitis” refers to the inflammation of the liver, and in this chapter the five so-called major or primary viruses that cause this inflammation are described. These are the viruses hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis delta virus (HDV), and hepatitis E virus (HEV). In Table 1, the characteristics of these hepatitis viruses are described. Although there are also secondary viruses that can infect the liver and cause hepatitis, such as cytomegalovirus, Epstein-Barr virus, herpes simplex virus 1, and enterovirus, the five primary viruses account for at least 95% of hepatitis virus infections. They primarily cause an infection of the liver and may infect other organs, while the secondary viruses infect the liver only during the course of a systemic infection.

Typical course of the virological and immunological manifestations of HAV (top) and HEV (bottom). Neither of these viruses results in a chronic infection in the immunocompetent host. Infections with both viruses are in most cases asymptomatic. The virological parameters for both viruses are very similar. Both viruses are transmitted through the fecal-oral route.

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FIGURE 1

Typical course of the virological and immunological manifestations of HAV (top) and HEV (bottom). Neither of these viruses results in a chronic infection in the immunocompetent host. Infections with both viruses are in most cases asymptomatic. The virological parameters for both viruses are very similar. Both viruses are transmitted through the fecal-oral route.

Virological profiles observed in patients infected with HBV. (A) Typical profiles in individuals with an acute HBV infection and subsequent resolution of the infection. HBV DNA is detected during a limited period of time and is ultimately undetectable using molecular techniques. Similarly, HBsAg is not detected anymore. The resolution of the infection and symptoms results in the presence anti-HBsAg antibodies, which is a marker for protection. (B) Profiles observed in individuals with a chronic HBV infection. In these cases, HBsAg and anti-HBc remain positive, while the patterns of HBeAg and anti-HBeAg may vary in time. The latter might be absent in the case of a precore mutation. HBV DNA is detectable at high levels during the whole period of the chronic infection.

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FIGURE 2

Virological profiles observed in patients infected with HBV. (A) Typical profiles in individuals with an acute HBV infection and subsequent resolution of the infection. HBV DNA is detected during a limited period of time and is ultimately undetectable using molecular techniques. Similarly, HBsAg is not detected anymore. The resolution of the infection and symptoms results in the presence anti-HBsAg antibodies, which is a marker for protection. (B) Profiles observed in individuals with a chronic HBV infection. In these cases, HBsAg and anti-HBc remain positive, while the patterns of HBeAg and anti-HBeAg may vary in time. The latter might be absent in the case of a precore mutation. HBV DNA is detectable at high levels during the whole period of the chronic infection.

Virological profiles observed in patients infected with HCV: the course of an HCV infection and the immunological events that follow. Most patients become chronically infected, while a limited number are able to resolve the infection spontaneously. Many patients, whether acutely or chronically infected, do not know that they are infected or are having overt signals of the disease. They do, however, follow these patterns and those who are chronically infected will have clinical symptoms later in life.

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FIGURE 3

Virological profiles observed in patients infected with HCV: the course of an HCV infection and the immunological events that follow. Most patients become chronically infected, while a limited number are able to resolve the infection spontaneously. Many patients, whether acutely or chronically infected, do not know that they are infected or are having overt signals of the disease. They do, however, follow these patterns and those who are chronically infected will have clinical symptoms later in life.

Virological profiles observed in patients infected with HDV. There are two routes of HDV infections. (Top) In the first one, HBV and HDV coinfect the same individual at the same time. Since the individual has not been infected previously with HBV, the replication of HBV and the production of HBsAg control the replication of HDV. As soon as the level of HBsAg is reduced due to the presence of anti-HBsAg, the replication of both HBV and HDV is dramatically reduced, and eventually both HBV DNA and HDV RNA are no longer detected in serum or plasma. Anti-HDV antibodies are present. (Bottom) In the case of a superinfection, HDV replication is enhanced from the beginning since an abundant amount of HBsAg is present in the liver. HDV RNA is detected by real-time amplification technologies as long as HBV replication and thus the production of HBsAg continue. In the case of this chronic infection with HDV, anti-HDV is also detected.

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FIGURE 4

Virological profiles observed in patients infected with HDV. There are two routes of HDV infections. (Top) In the first one, HBV and HDV coinfect the same individual at the same time. Since the individual has not been infected previously with HBV, the replication of HBV and the production of HBsAg control the replication of HDV. As soon as the level of HBsAg is reduced due to the presence of anti-HBsAg, the replication of both HBV and HDV is dramatically reduced, and eventually both HBV DNA and HDV RNA are no longer detected in serum or plasma. Anti-HDV antibodies are present. (Bottom) In the case of a superinfection, HDV replication is enhanced from the beginning since an abundant amount of HBsAg is present in the liver. HDV RNA is detected by real-time amplification technologies as long as HBV replication and thus the production of HBsAg continue. In the case of this chronic infection with HDV, anti-HDV is also detected.

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